Smokeless Tobacco and Cigar and/or Pipe Are Risk Factors for Barrett Esophagus in Male Patients With Gastroesophageal Reflux Disease

Objective

To investigate the effect of smokeless tobacco (ST), cigar and/or pipe smoking (CP) on the development of Barrett esophagus (BE) in white male patients with gastroesophageal reflux disease (GERD).

小柴胡汤联合环磷酰胺对腹水瘤细胞株肝癌小鼠肿瘤间质血管生成影响随机平行对照研究

[目的]观察小柴胡汤联合环磷酰胺对腹水瘤细胞株(EAC)肝癌小鼠体重、肿瘤间质血管生成影响。[方法]使用随机平行对照方法,将40只昆明小鼠,采用完全随机化分组方法分为模型组、中药组、西药组、联合组,每组10只。各组皮下注射浓度为2.0×106/ml的EAC肝癌小鼠细胞株0.2ml/只造模,分别给予小柴胡汤、环磷酰胺、小柴胡汤+环磷酰胺灌胃。免疫组化法检测血管内皮生长因子(VEGF)表达、光镜下观察形态学改变,透射电镜观察肿瘤组织血管生成。[结果]中药组、西药组、联合组VEGF阳性表达,瘤组织内的VEGF蛋白表达阳性率和平均染色强度均低于模型组(P<0.01),联合组最明显。光镜下显示:中药组、西药组、联合组肿瘤间质毛细血管数量均减少,联合组最为明显,中药组次之。电镜下显示:中药组、联合组都可以破坏肿瘤组织内新生毛细血管结构,联合组破坏最严重。[结论]小柴胡汤联合环磷酰胺可降低EAC肝癌小鼠瘤组织中VEGF蛋白表达;、抑制肿瘤间质血管生长。     

槲皮素逆转EAC／ADR抗药性的研究

本研究结果提示，槲皮素具有增强ＡＤＲ对ＥＡＣ和ＥＡＣ／ＡＤＲ的作用。大剂量槲皮素（５０ｍｇ／ｋｇ）能使ＥＡＣ及ＥＡＣ／ＡＤＲ小鼠的生存期显著延长，生命延长率分别依次为１３４．４±５．１％及６８．８±３．５％；而用槲皮素６．２５及１２．５ｍｇ／ｋｇ时，小鼠生命延长率不明显，但与ＡＤＲ１ｍｇ／ｋｇ合用时，使ＥＡＣ及ＥＡＣ／ＡＤＲ小鼠生命延长率分别提高到７３．９±３．７％，１００．６±５．９％及４９．７±３．１％，８４．１±５．１％。从上述结果看出，槲皮素对逆转ＥＡＣ／ＡＤＲ的抗药性是有一定作用的。     

Importance of factors H and I for the adherence of C3b-coated erythrocytes to cells

The role of cell membrane-associated human factor H for the binding of cell-bound C3b to complement receptor-carrying (CR+) cells was investigated. Pretreatment of CR+ cells with antibodies to factor H inhibited the adherence of C3b-coated red cells to human tonsil lymphocytes (TL) and peripheral blood monocytes (M phi). The C3b receptor reactivity of human polymorphonuclear leucocytes (PMN) was not influenced and the one of Raji lymphoblastoid cells only slightly influenced; iC3b and C3d receptor reactivity was in no case affected. When diisopropylfluorophosphate (DFP) in a concentration of 0.1 mM was present during pretreatment of the CR+ cells with anti H, the antibodies gained the capacity to inhibit the adherence of C3b-coated erythrocytes to Raji cells; this effect was dose-dependent with respect to DFP. In contrast, there was no influence of DFP on the inhibition pattern of anti H in the case of TL and M phi. The adherence of C3b-coated erythrocytes to PMN remained unaffected by anti-H antibodies in the presence of DFP. Polyclonal as well as monoclonal antibodies directed against human factor I inhibited the binding of C3b cells to Raji cells but not to TL. Additionally, when anti I and anti H antibodies were both present, C3b receptor reactivity of Raji cells was inhibited to a larger extent than with either antibody alone; again, TL remained unaffected. Results obtained by washing the Raji cells before and after treatment with anti H and anti I suggest that the respective antibodies act on factor H primarily on the level of the cell membrane and on factor I in the fluid phase.     

Sequential changes of the T lymphocytes following ER rosette formation in guinea pigs. I. Expression of Fc and complement receptors

Changes in proportions of the Fc and complement receptor (FcR, CR) positive T lymphocytes from guinea pigs following their interaction with rabbit erythrocytes (ER) were studied using EA and EAC rosette forming assays. Significant increases in the percentages of EA and EAC rosette forming cell (RFC) were observed when thymocytes or lymph node cells were assayed after ER rosette formation. Furthermore, T-enriched fraction by the ER monolayer adherence technique also showed similar or somewhat higher increases in the proportions of both EA and EAC RFC than those of unfractionated cells after contact with ER. The double rosette assay by ER with EA or EAC showed that 50-80% of the Fc and/or complement receptor positive lymphocytes bound rabbit erythrocytes simultaneously. These findings strongly suggest that at least a subset of the guinea pig T cells is altered to express Fc and/or complement receptors on their surfaces following the interaction with ER.     

Cleavage of membrane-bound C3b and C3bi by viable human neutrophils (PMN)

Cleavage of C3 by purified leukocyte enzymes and crude extracts of human polymorphonuclear leukocyte (PMN) granules has been reported. We demonstrate that viable PMN mediate the cleavage of erythrocyte-bound C3b and C3bi via cell-associated proteases. Greater than 50% of 125IC3(x) was released from EAC43bix during a 5-min incubation with viable PMN at 37 degrees C. More than a 30-min incubation was required for substantial release from EAC43bx. Culture fluids from PMN suspensions had limited cleaving ability; cleavage of cell-bound C3bx and C3bix was only partially reduced when PMN were preincubated with high levels of soluble C3 which completely blocked EAC43b rosettes. Thus, cell-to-cell contact between opsonized erythrocytes and viable PMN with surface-associated proteases are responsible for cleavage of these opsonic sites. The effect of defined protease inhibitors on PMN cleaving activity as well as on purified leukocyte elastase was examined. Phenylmethylsulfonyl fluoride (PMSF) and the leukocyte elastase inhibitor, methoxy-succinate-alanine-alanine-valine-chloromethyl ketone (MeO) each inhibited cleavage of C3b by 90% and C3bi by 60%. In contrast, the cathepsin-G inhibitor, benzyloxy-carbonyl-glycine-leucine-phenylalanine-chloromethyl ketone (Z) inhibited C3b and C3bi cleavage by less than 20 and less than 5%, respectively. Ethylenediaminetetra-acetate (EDTA), which had a minimal effect on soluble leukocyte elastase, also inhibited PMN-related release. Thus, elastase appeared to be the principle but not the only enzyme responsible for cleavage of C3b and C3bi. PMSF and MeO had a minimal effect on the activity of purified C3bINA (Factor I); and PMN-mediated release of C3b fragments was not inhibited by anti-Factor I and anti-beta 1H (Factor H) IgG and Fab. Thus, these control proteins are not involved in the PMN-mediated cleavage under study. PMN-mediated cleavage of C3b was also inhibited when PMSF- and MeO-treated PMN were washed to remove the fluid phase phase protease inhibitor before adding EAC43b. This suggests that proteases localized in the PMN membrane, prior to the adherence of EAC43b, are responsible for C3b cleavage. Normal human serum was effective in blocking PMN-mediated release activity, while serum from alpha 1 antitrypsin-deficient patients was minimally effective. This suggests a mechanism for the in vivo regulation of PMN-mediated release of C3b and C3bi from opsonized particles by the natural plasma protease inhibitors.     

魔芋对艾氏腹水瘤(EAC)抑制作用的研究

 目的　探讨魔芋对肿瘤的抑制作 用及对免疫功能的影响。方法　分别将魔芋精粉(RKM),魔芋灰粉、新鲜魔 芋茎块煎剂,环磷酰胺、生理盐水对艾氏腹水瘤(EAC)小鼠灌胃给药。结果　各实验组与盐水对照组相比有明显的抑瘤作用,能延长小鼠的生存时间,同时对动物白 细胞无影响,并能增加淋巴细胞转化率。结论　魔芋可能是通过增强机体免 疫功能来抑制移植性肿瘤的生长,起到抗肿瘤作用。     

4,6-苄叉基-D-葡萄糖抗癌作用的研究

本文证明,4、6-苄叉基-D-葡萄糖(BG)i·p,50、100mg/kg对Walker 256和62.5、125mg/kg对EAC实体型移植性肿瘤均有明显抑制作用,对HepA实体型和EAC腹水型则无抑癌活性。体外实验表明,BG 100μg/ml对Hela细胞无活性,200μg/ml对EAC细胞有一定抑制作用。BG i.v LD_(50)为200mg/kg以上。i.p 350mg/kg以上。     

硫酸壳聚糖体内抗肿瘤作用的实验研究

目的：研究硫酸壳聚糖的体内抗肿瘤作用。方法：用高、低（200、100mg/kg）两个剂量的硫酸壳聚糖分别腹腔注射治疗肉瘤180（S180）小鼠和艾氏腹水癌（EAC）小鼠10d,然后测定其抑瘤率、重要器官的内脏指数和生命延长率,同时设生理盐水组（空白对照组）和氟尿嘧啶组（阳性对照组）进行比较。结果：硫酸壳聚糖高、低剂量组和氟尿嘧啶组的抑瘤率分别为38.67%、30.19%和43.27%,3组的生命延长率分别为65.38%、69.23%和54.93%。和生理盐水组、氟尿嘧啶组相比,硫酸壳聚糖高、低剂量组的S180小鼠的胸腺指数均有明显增加（P〈0.05）。结论：硫酸壳聚糖能有效抑制S180小鼠肿瘤的生长和延长EAC小鼠的生存时间,其作用机制可能与其提高机体的免疫力有关。     

荔枝核对小鼠S180、EAC肿瘤细胞Bax和Bcl-2蛋白表达的影响研究

目的:研究荔枝核对小鼠S180、EAC肿瘤细胞Bax和Bcl-2蛋白表达的影响。方法:采用小鼠腋下接种瘤株的方法,复制EAC、S180及肝癌荷瘤动物模型。小鼠EAC、S180细胞与肝癌细胞混悬液分别用生理盐水按1∶1进行稀释,制成含瘤腹水混悬液。小鼠在给药前24h进行腋窝皮下接种,每只0·2mL,整个操作在无菌条件下60min内完成。连续给药10d,观察EAC、S180肿瘤和肝癌肿瘤细胞的生长情况。结果:荔枝核能够显著抑制EAC、S180肿瘤和肝癌肿瘤细胞的生长。结论:荔枝核具有抑制小鼠EAC、S180、肝癌细胞的作用;具有抑制小鼠S180、EAC体内、外细胞生长的作用;并能促进肿瘤细胞凋亡,从而发挥抗肿瘤的作用。